Taste helps establish food preference and the neural processing of taste aspect of food reward starts from the gustatory system. The gustatory information via cranial nerves reaches the brain first in the nucleus of the solitatory tract (NST). Parabrachial nucleus (PBN) receives the excitatory glutamatergic input from the NST and has been shown to control feeding. In addition, PBN is also necessary to convey hedonic information of taste stimuli. Given that PBN sends substantial projections to midbrain dopamine neurons, it raises the possibility that taste stimuli may engage dopamine neurons in the ventral tegmental area (VTA) via PBN to modulate food intake. Thus, in the The release of noradrenaline in midbrain monoaminergic nuclei, including the dorsal raphe nucleus (DR), ventral tegmental area (VTA), and substantia nigra pars compacta (SNc) excites serotonin and dopamine neurons through the activation of excitatory 1-adrenergic receptors, enhancing action potential firing and neurotransmitter release. The release of noradrenaline from axon terminals is through the activation of inhibitory 2-adrenergic receptors. Despite this influential role, the most basic questions regarding noradrenaline-dependent excitation remain unanswered, stemming from an incomplete characterization of 1- and 2-adrenergic receptor signaling at a synaptic level and within the context of the brain circuits and behavior. We have been using wild type mice for acute brain slice electrophysiology to determine the signal transduction pathway and spatial and temporal kinetics of 1-adrenergic receptor signaling in the DR. A manuscript detailing the results of these studies is in preparation. In addition, intracranial microinjections of retrograde neural tracers have been made in the DR of wild type mice, followed by transcardial perfusion and histological experiments in order to determine the origin of noradrenaline axon terminals in the DR. Activation of 1-adrenergic receptors in the DR by dopamine released from midbrain dopamine neuron axon terminals has been examined by intracranial microinjection of viral vectors encoding for the selective expression of light-activated channelrhodopsin 2 (AAV-DIO-ChR2-eYFP) in the SNc/VTA of TH-cre mice. Functional connectivity was assessed by acute brain slice electrophysiology.